title: Human mesenchymal stem cells from adipose tissue and amnion influence T-cells depending on stimulation method and presence of other immune cells.
abstract: Mesenchymal stem cells (MSCs) are multipotent progenitor cells exerting immunomodulatory effects on cells of the innate and adaptive immune system. It has been shown that an inflammatory milieu is required for the activation of MSC-mediated immunomodulation, and interferon-γ (IFN-γ) plays an important role in this process. We determined the influence of IFN-γ on human adipose-derived stem cells (ASCs) and human amniotic mesenchymal stromal cells (hAMSCs). We further evaluated the effect of MSCs on stimulated T-cells and peripheral blood mononuclear cells (PBMCs) in a cell-contact independent setting. On IFN-γ treatment, ASCs and hAMSCs possessed significantly higher antiproliferative properties and showed surface characteristics of nonprofessional antigen presenting cells (HLA-DR(+)CD40(med+)CD54(high)) with a possible regulatory phenotype (PD-L1(+)PD-L2(+)). The effect of ASCs and hAMSCs on cytokine secretion and T-cell activation was dependent on stimulation method and cellular context. Although ASCs and hAMSCs highly inhibited cytokine secretion of stimulated PBMCs, this was not observed in the case of purified T-cells. The presence of ASCs even favored the secretion of pro-inflammatory cytokines including IFN-γ by T-cells, although T-cell proliferation was efficiently inhibited. Further, ASCs enhanced the number of CD69(+) T-cells independent of the stimuli and cellular context. Interestingly, ASCs significantly suppressed CD25 expression on phytohemagglutinin stimulated PBMCs but had no effect on αCD3/αCD28 stimulated cells. Depending on the stimulation method and cellular context, immune cells create a specific cytokine milieu in vitro, thus differently influencing MSCs and, in turn, affecting their action on immune cells.
authors.affiliation: Red Cross Blood Transfusion Service of Upper Austria, Linz, Austria.
authors.forename: Barbara
authors.initials: B
authors.lastname: Kronsteiner
authors.forename: Susanne
authors.initials: S
authors.lastname: Wolbank
authors.forename: Anja
authors.initials: A
authors.lastname: Peterbauer
authors.forename: Christa
authors.initials: C
authors.lastname: Hackl
authors.forename: Heinz
authors.initials: H
authors.lastname: Redl
authors.forename: Martijn
authors.initials: M
authors.lastname: van Griensven
authors.forename: Christian
authors.initials: C
authors.lastname: Gabriel
mesh_terms: D000273:Adipose Tissue / Q000166:cytology*; D000650:Amnion / Q000166:cytology*; D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D002450:Cell Communication / Q000187:drug effects; D018929:Cell Culture Techniques / Q000379:methods*; D049109:Cell Proliferation / Q000187:drug effects; D002469:Cell Separation; D018925:Chemokines / Q000378:metabolism; D018920:Coculture Techniques; D015232:Dinoprostone / Q000378:metabolism; D006684:HLA-DR Antigens / Q000276:immunology; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007371:Interferon-gamma / Q000494:pharmacology; D037181:Lectins, C-Type / Q000378:metabolism; D008213:Lymphocyte Activation / Q000187:drug effects; D018655:Lymphocyte Count; D059630:Mesenchymal Stem Cells / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D012995:Solubility / Q000187:drug effects; D013601:T-Lymphocytes / Q000166:cytology* / Q000187:drug effects / Q000276:immunology*; D015854:Up-Regulation / Q000187:drug effects; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D018925:Chemokines; D015232:Dinoprostone; D006684:HLA-DR Antigens; D018799:Intercellular Adhesion Molecule-1; D007371:Interferon-gamma; D037181:Lectins, C-Type; D000099192:CD69 Antigens